Exercise capacity is reduced in humans with congestive heart failure but the underlying mechanisms are unclear. Currently it is believed that the inability of the cardiovascular and pulmonary systems to deliver adequate oxygen to exercising muscles reduces motor capacity. Preliminary experiments that I conducted demonstrate that acute elevations of left atrial pressure inhibit rhythmic locomotor activity in decerebrate cats. I was also able to show that a vagal reflex mediates the inhibition since cutting the cervical vagi abolished the response. These findings suggest that a neural mechanism can contribute to the reduced exercise capacity observed in humans with congestive heart failure. The proposed experiments have two goals. The first is to identify the location of vagal nerve endings and the type of vagal nerve fibers that comprise the afferent arm of this viscerosomatic reflex. The second goal is to define a segment of the central pathway and the mechanisms by which vagal afferent input inhibits exercise. These experiments will be performed in a decerebrate, unanesthetized cat capable of producing rhythmic locomotor activity in response to stimulation of the midbrain mesencephalic locomotor region. A balloon placed in the left atrium will be inflated to raise left atrial pressure and create pulmonary circulatory congestion. The stimulus produced by balloon inflation will be isolated to the lung by blocking cardiac afferents with lidocaine. Differential cooling of the vagus will be used to determine the vagal fibers mediating the reflex inhibition of exercise. The possibility that the ventral and/or dorsal tegmental fields of the pons contribute to the central integration of this viscerosomatic reflex will be investigated. These two brainstem sites act reciprocally: the ventral tegmental field facilitates locomotion and the dorsal tegmental field suppresses locomotion. Subthreshold electrical stimulation will be applied to the ventral tegmental field during the reflex inhibition of locomotion. The resumption of locomotion will indicate that vagal afferent input inhibits this excitatory region. In addition, excitatory amino acid receptor antagonists will be microinjected into the dorsal tegmental field during the reflex inhibition of locomotion. The resumption of locomotion will indicate that vagal afferent input excites this inhibitory region. These studies will contribute to our understanding of the mechanisms that underlie exercise intolerance in patients with congestive heart disease.